Amorfix Life Sciences develops two vaccines that extend life in amyotrophic lateral sclerosis (ALS) animal model
Amorfix Life Sciences announced that it will be presenting the results from its vaccine development program for amyotrophic lateral sclerosis (ALS), commonly referred to as Lou Gehrig's disease, at the 132nd Annual Meeting of the American Neurological Association today in Washington, DC. The vaccine approach, also known as active immunization, is the second therapeutic approach for which proof-of-concept has been established by Amorfix for the treatment of ALS this year. In March, Amorfix established a passive immunization approach in the same mouse model of ALS by injecting monoclonal antibodies that target the misfolded superoxide dismutase 1(SOD1) protein.
The paper entitled "Active and Passive Immunization of SOD1 Disease Specific Epitopes in a Mouse Model of Amyotrophic Lateral Sclerosis" will be presented by Dr. Neil Cashman, the Chief Scientific Officer of Amorfix. The study shows for the first time life extension in a mouse model of ALS using two vaccines targeted at different regions of the protein, termed disease-specific epitopes, found only on the molecular surface of misfolded SOD1.
"These results support our original belief that specifically targeting misfolded proteins using immunotherapies may lead to an effective treatment for this debilitating disease, and by extension numerous other diseases such as Parkinson's and Alzheimer's diseases," said Dr. George Adams, CEO of Amorfix Life Sciences.
Amorfix's targeted vaccine approach is based on the premise that the misfolding and aggregation of SOD1, which is known to occur in familial ALS patients, is a principal agent in the death of motor neurons in all types of ALS disease. Amorfix believes that by administering a vaccine designed to elicit the production of antibodies that target only misfolded SOD1, the immune system could be educated to specifically recognize misfolded SOD1 as foreign and neutralize it, while sparing the normally folded protein from autoimmune recognition.
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